Sure, I can provide references, though I provided links which make it easy to look up references. in the case of ta-65 you can look it up in wiki and use those references since the references provided by the supplement company would likely be more biased. He also claimed I was regurgitating supplement advertisements and I dont think I come across like that at all. I think in this case its just sloppy laziness on his part so I didn't feel like making any effort.

“Forget Jesus, the stars died so you could be born.” - Lawrence M. Krauss

(07-02-2014 05:57 AM)DeepThought Wrote: What about supplements like astragalus extracts - including the ridiculously expensive ta-65 supplement that has a fair amount of science behind it.

RevGenetics is the dude I get my resveratrol and curcumin from. He's more expensive than most but provides an independent COA for all of his raw ingredients. He's thrown batches away which were contaminated with mercury and other shit. That's worth it to me.

I looked into TA-65 but what scared me was that almost all cancer cells are characterized by increased telomerase activity. If there are any cancer cells floating around looking for some buddies to throw a tumor party why wouldn't TA-65 or other similar supplements increase their telomerase activity as well? That and the fact that after nearly a decade there are still no animal studies showing TA-65 increases lifespan turned me off of it.

(07-02-2014 05:57 AM)DeepThought Wrote: What about supplements like astragalus extracts - including the ridiculously expensive ta-65 supplement that has a fair amount of science behind it.

I looked into TA-65 but what scared me was that almost all cancer cells are characterized by increased telomerase activity. If there are any cancer cells floating around looking for some buddies to throw a tumor party why wouldn't TA-65 or other similar supplements increase their telomerase activity as well? That and the fact that after nearly a decade there are still no animal studies showing TA-65 increases lifespan turned me off of it.

You are right. More than 90% of cancer cells have telomerase switched on, whereas the other 10% have an alternative pathway to maintain telomere length.

As I had mentioned in my initial post, chromosomes shorten with every cell division. And telomerase is the protein that elongates the end of chromosomes and therefore maintains telomere (greek for "end piece") length.

The reason why we have evolved to have telomerase switched off is because if it was switched on, our ancestors would have died from cancer before they reached the age of reproduction. In general, traits that display a phenotype after the age of reproduction are not under the pressure of selection. Telomerase is one example. Inactive telomerase is beneficial before the age of reproduction (due to avoiding cancer) but becomes detrimental at a later stage (due to aging).

I will explain why active telomerase leads to cancer for those who are interested:

Cancer cells are cells, which have accummulated mutations that mess with their cellular regulation. The first check-point for a cancer cell is to accummulate DNA mutations, which switch off pathways that would normally sense DNA damage and initiate cell death (apoptosis) or cellular senescence. After passing that check-point, cancer cells have to pass the second check-point: because telomerase is switched off in all somatic cells, cancer cells need to accumulate mutations that switch it on again. If the cancer cell does not manage to do so, it will divide and divide and the chromosomes will become shorter and shorter. Eventually, the chromosome length will be so short that it will lead to genomic instability and cell death.

There are more check-points, but I won't mention them now. But in essence, those check-points are there to protect us from the formation of cancer.

I hope now it is clear that anything that switches on telomerase activity is cancerogenic.

(07-02-2014 05:42 PM)GirlyMan Wrote: I looked into TA-65 but what scared me was that almost all cancer cells are characterized by increased telomerase activity. If there are any cancer cells floating around looking for some buddies to throw a tumor party why wouldn't TA-65 or other similar supplements increase their telomerase activity as well? That and the fact that after nearly a decade there are still no animal studies showing TA-65 increases lifespan turned me off of it.

You are right. More than 90% of cancer cells have telomerase switched on, whereas the other 10% have an alternative pathway to maintain telomere length.

As I had mentioned in my initial post, chromosomes shorten with every cell division. And telomerase is the protein that elongates the end of chromosomes and therefore maintains telomere (greek for "end piece") length.

The reason why we have evolved to have telomerase switched off is because if it was switched on, our ancestors would have died from cancer before they reached the age of reproduction. In general, traits that display a phenotype after the age of reproduction are not under the pressure of selection. Telomerase is one example. Inactive telomerase is beneficial before the age of reproduction (due to avoiding cancer) but becomes detrimental at a later stage (due to aging).

I will explain why active telomerase leads to cancer for those who are interested:

Cancer cells are cells, which have accummulated mutations that mess with their cellular regulation. The first check-point for a cancer cell is to accummulate DNA mutations, which switch off pathways that would normally sense DNA damage and initiate cell death (apoptosis) or cellular senescence. After passing that check-point, cancer cells have to pass the second check-point: because telomerase is switched off in all somatic cells, cancer cells need to accumulate mutations that switch it on again. If the cancer cell does not manage to do so, it will divide and divide and the chromosomes will become shorter and shorter. Eventually, the chromosome length will be so short that it will lead to genomic instability and cell death.

There are more check-points, but I won't mention them now. But in essence, those check-points are there to protect us from the formation of cancer.

I hope now it is clear that anything that switches on telomerase activity is cancerogenic.

It's not always that simple though. Eg: some types of prostate cancer are cause by cells that keep divididing after the telomeres fray to nothing. The resulting genetic damage causes cancer also. Different cell lines express different genes and have different behaviour when the chromosome ends start fraying.

It is very simplistic to say that anything that turns on telomerase production causes cancer since regular exercise activates telemerase along with many other genes that promote cell repair and autophagy. Cancer cant be put in a simple little box like that otherwise we would have cured it by now.

The naked mole rat... need I say more?

Astragalus extract has extended health span in animal models. I would think that something cancerogenic wouldn't do that...

“Forget Jesus, the stars died so you could be born.” - Lawrence M. Krauss

(30-01-2014 07:28 PM)BrokenQuill92 Wrote: Am I too young to start using anti-aging treatments? And do they even work?

Some anti-aging stuff works, some are nothing more than over-expensive scams.

Personally I don't see much of a point to using 'anti-aging' stuff.

Who is really so afraid of aging or vain and frightened of the idea that they are no longer young? Seems pretty pointless to me regardless of your age, but I'm just a young guy so what do I know about this sort of stuff

The people closely associated with the namesake of female canines are suffering from a nondescript form of lunacy.
"Anti-environmentalism is like standing in front of a forest and going 'quick kill them they're coming right for us!'" - Jake Farr-Wharton, The Imaginary Friend Show.

I keep things simple on purpose for people who do not have any education in this field to grasp the basics.

All cancer cells that are not telomerase active have the ALT mechanism to maintain telomere length. There is no viable cancer cell line, that does not have either one of those mechanisms. (if you persist, please provide a source)

And it is quite reasonable and easy to understand, really:
- During every cell division, chromosomes shorten
- When telomeres (chromosome capping structures) diminish, the naked chromosome ends are recognized as double strand breaks and are subjected to DNA recombination (meaning two ends from two chromosomes are "glued" together)
- the recombination gives rise to fused chromosomes with more than one centromere
- during the next cell division, these chromosomes are then sheared apart during Anaphase, which causes genomic instability and leads to cell death

- Cancer cells proliferate uncontrollably
- if cancer cells do not activate a mechanism to maintain chromosome length, they will die due to what is described above

Telomerase inactivity in our somatic cells serves as a check-point to prevent cancer cells from proliferating. And this is the consensus in the field.

(08-02-2014 07:10 AM)Youkay Wrote: Every paper on pubmed will give you the same insight: 90% of cancer cells are telomerase active, 10% have an ALT mechanism to maintain telomere length. You can also look it up in biochemistry books.